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作 者:李鹏[1] 易斌[1] 王秀琼[1] 罗铁山[1] 石胜驰[1] 许广明[1] 陶国才[1]
机构地区:[1]第三军医大学第一附属医院手术麻醉科,重庆400038
出 处:《中国老年学杂志》2009年第23期3064-3066,共3页Chinese Journal of Gerontology
摘 要:目的研究异氟醚对老年大鼠脑组织高级糖基化终末产物(AGEs)及氧化应激水平的影响。方法老年及成年SD雄性大鼠共32只,在安静无干扰环境中进行12h/12h光暗周期节律适应4d后,随机分为老年对照组(N1组),老年异氟醚处理组(A1组),成年对照组(N2组),成年异氟醚处理组(A2组)。异氟醚组均给予异氟醚吸入处理3h,对照组在相同时间,安静环境呼吸空气3h。免疫组织化学法测定大鼠海马AGEs水平变化,硫代巴比妥法(TBA)测定脑组织丙二醛(MDA)含量,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性。结果与N2组比较,N1组大鼠脑内AGEs、MDA基础水平较高,SOD活性低于N2组。24h后A1组海马AGEs水平较N1组及A2组明显升高(P<0.01);A2组AGEs水平与N2组比较无显著变化(P>0.05)。A1组MDA含量为(10.35±0.62)nmol/mg,较N1组及A2组明显升高,而SOD活性降低(P<0.01)。A2组SOD活性为(104.45±11.26)U/mg,较N2组降低,而MDA活性较A2组升高(P<0.05)。结论异氟醚处理可引起老年大鼠脑组织内AGEs增高及氧化应激水平进一步升高可能是老年术后认知功能紊乱的机制之一。Objective To investigate the effects of isoilurane on advanced glyeation end products (AGEs) and oxidative stress levels in the rat brain. Methods 32 male SD rats were randomly divided into 4 groups: old age control group( N1 ), old isoflurane anesthesia group( A1 ) , adult control group(N2) , adult isoflurane anesthesia group (A2). Anesthesia groups were given inhaled isoflurane anesthesia for 3 hours meanwhile breathing the air in the control group. The animals were killed 24 hours after anesthesia to detect the AGEs in the hip- pocampus tissues by immunohistochemistry. Brain tissue malondialdehyde(MDA) and superoxide dismutase(SOD) were detected by colorimetric. Results Compared with N2 group, the basis of the levels of AGEs and MDA were higher but SOD activity was lower in N1 group. Compared with N1 and A2 group, the hippocampal levels of AGEs were significantly higher in group A1 after 24 hours (P 〈0. 01 ). There was no significant difference in AGEs levels between N2 and A2 group ( P 〉 0.05 ). Compared with N1 and A2 group, MDA increased signif- icantly and SOD activity decreased in A1 group (P 〈 0. 01 ). Compared with N2 group, MDA were higher and SOD activity were lower in A2 group( P 〈 0.05 ). Conclusions Isoflurane can increase the expression of AGEs and the levels of oxidative stress in hippoeampus of aged rats. The changes may be one of the mechanisms of old postoperative cognitive dysfunction patients.
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